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Article: Interplay of pituitary adenylate cyclase-activating polypeptide with a silencer element to regulate the upstream promoter of the human gonadotropin-releasing hormone receptor gene

TitleInterplay of pituitary adenylate cyclase-activating polypeptide with a silencer element to regulate the upstream promoter of the human gonadotropin-releasing hormone receptor gene
Authors
KeywordscAMP
Gene regulation
Gonadotrope
Human GnRH receptor
Human reproduction
PACAP
Promoter
Silencer
Issue Date2001
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/mce
Citation
Molecular And Cellular Endocrinology, 2001, v. 176 n. 1-2, p. 135-144 How to Cite?
AbstractMultiple transcription start sites were identified in the human gonadotropin releasing hormone receptor (hGnRHR) gene. Recently, an upstream promoter residing at -1727/-1674, in vicinity of a CAP site at -1673, was characterized. In this report, we elucidated the underlying mechanisms for the regulation of this promoter. Functionally, this promoter was constitutively suppressed by a silencer element (-1673/-1351) situated immediately downstream to it. On the other hand, pituitary adenylate cyclase-activating polypeptide (PACAP), via the cAMP pathway, was found to be the extracellular cue to control the upstream promoter. Following PACAP-27, PACAP-38 (30 nM) and forskolin (25 μM) treatment, there were significant increases in the reporter gene activities. By deletion analysis, the region residing at -1727 to -1577, containing the distal promoter and 97 bp of the silencer was subsequently found to be responsible for PACAP/cAMP induction. To localize the PACAP-dependent cis-acting element(s) within the silencer, block replacement scanning mutation was performed and a hGnRHR gene PACAP-responsive element (GPRE) was identified at -1676/-1648. The actions of PACAPs and forskolin on the GPRE were further evidenced by gel mobility shift assays. There was an increase in protein binding onto this element only after peptide treatment. As GnRH receptor number on gonadotrope cell surface is a key factor in regulating gonadotropin release, the present study provides an insight into the interplay between PACAP and GnRH receptors on pituitary gonadotropes to control human reproductive functions. Copyright © 2001 Elsevier Science Ireland Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/84754
ISSN
2023 Impact Factor: 3.8
2023 SCImago Journal Rankings: 1.130
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorNgan, ESWen_HK
dc.contributor.authorLeung, PCKen_HK
dc.contributor.authorChow, BKCen_HK
dc.date.accessioned2010-09-06T08:56:43Z-
dc.date.available2010-09-06T08:56:43Z-
dc.date.issued2001en_HK
dc.identifier.citationMolecular And Cellular Endocrinology, 2001, v. 176 n. 1-2, p. 135-144en_HK
dc.identifier.issn0303-7207en_HK
dc.identifier.urihttp://hdl.handle.net/10722/84754-
dc.description.abstractMultiple transcription start sites were identified in the human gonadotropin releasing hormone receptor (hGnRHR) gene. Recently, an upstream promoter residing at -1727/-1674, in vicinity of a CAP site at -1673, was characterized. In this report, we elucidated the underlying mechanisms for the regulation of this promoter. Functionally, this promoter was constitutively suppressed by a silencer element (-1673/-1351) situated immediately downstream to it. On the other hand, pituitary adenylate cyclase-activating polypeptide (PACAP), via the cAMP pathway, was found to be the extracellular cue to control the upstream promoter. Following PACAP-27, PACAP-38 (30 nM) and forskolin (25 μM) treatment, there were significant increases in the reporter gene activities. By deletion analysis, the region residing at -1727 to -1577, containing the distal promoter and 97 bp of the silencer was subsequently found to be responsible for PACAP/cAMP induction. To localize the PACAP-dependent cis-acting element(s) within the silencer, block replacement scanning mutation was performed and a hGnRHR gene PACAP-responsive element (GPRE) was identified at -1676/-1648. The actions of PACAPs and forskolin on the GPRE were further evidenced by gel mobility shift assays. There was an increase in protein binding onto this element only after peptide treatment. As GnRH receptor number on gonadotrope cell surface is a key factor in regulating gonadotropin release, the present study provides an insight into the interplay between PACAP and GnRH receptors on pituitary gonadotropes to control human reproductive functions. Copyright © 2001 Elsevier Science Ireland Ltd.en_HK
dc.languageengen_HK
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/mceen_HK
dc.relation.ispartofMolecular and Cellular Endocrinologyen_HK
dc.rightsMolecular and Cellular Endocrinology. Copyright © Elsevier Ireland Ltd.-
dc.subjectcAMPen_HK
dc.subjectGene regulationen_HK
dc.subjectGonadotropeen_HK
dc.subjectHuman GnRH receptoren_HK
dc.subjectHuman reproductionen_HK
dc.subjectPACAPen_HK
dc.subjectPromoteren_HK
dc.subjectSilenceren_HK
dc.subject.meshGene Silencing - drug effects-
dc.subject.meshNeuropeptides - pharmacology-
dc.subject.meshPromoter Regions, Genetic - genetics-
dc.subject.meshReceptors, LHRH - genetics-
dc.subject.meshResponse Elements - genetics-
dc.titleInterplay of pituitary adenylate cyclase-activating polypeptide with a silencer element to regulate the upstream promoter of the human gonadotropin-releasing hormone receptor geneen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0303-7207&volume=176&issue=1-2&spage=135&epage=144&date=2001&atitle=Interplay+of+pituitary+adenylate+cyclase-activating+polypeptide+with+a+silencer+element+to+regulate+the+upstream+promoter+of+the+human+gonadotropin-releasing+hormone+receptor+geneen_HK
dc.identifier.emailNgan, ESW: engan@hku.hken_HK
dc.identifier.emailChow, BKC: bkcc@hku.hken_HK
dc.identifier.authorityNgan, ESW=rp00422en_HK
dc.identifier.authorityChow, BKC=rp00681en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/S0303-7207(01)00402-6en_HK
dc.identifier.pmid11369453-
dc.identifier.scopuseid_2-s2.0-0035947399en_HK
dc.identifier.hkuros103895en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0035947399&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume176en_HK
dc.identifier.issue1-2en_HK
dc.identifier.spage135en_HK
dc.identifier.epage144en_HK
dc.identifier.isiWOS:000169103500017-
dc.publisher.placeIrelanden_HK
dc.identifier.scopusauthoridNgan, ESW=22234827500en_HK
dc.identifier.scopusauthoridLeung, PCK=55419381000en_HK
dc.identifier.scopusauthoridChow, BKC=7102826193en_HK
dc.identifier.issnl0303-7207-

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